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Campus lockdown policy is one of the most effective non-pharmaceutical intervention strategies used to prevent and control the coronavirus disease 2019epidemic worldwide. College students were greatly affected by this policy. Related studies center on English-speaking countries; few have highlighted discussion of the Chinese context. This study, therefore, aimed to broadly elicit the real experiences and unique insights of college students on Chinese campus lockdown policy. Through qualitative research, we identified four key themes with ten contributory subthemes: physiological experiences, safety experiences, love and belonging experiences, and self-esteem experiences. The unique contribution of this study relates to experiences relating to love and belonging and to self-esteem, which are little discussed in the existing literature. Our findings can provide enlightenment on how to improve college students’ health.

Alzheimer’s disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation has emerged as a central player in the onset and progression of AD. As innate lymphoid cells, natural killer (NK) cells orchestrate the initiation and evolution of inflammatory responses. Yet, the transcriptomic features of NK cells in AD remain poorly understood. We assessed the diversity of NK cells using web-based single-cell RNA sequencing data of blood NK cells from patients with AD and control subjects and flow cytometry. We identified a contraction of NK cell compartment in AD, accompanied by a reduction of cytotoxicity. Unbiased clustering revealed four subsets of NK cells in AD, i.e., CD56 bright NK cells, CD56 dim effector NK cells, adaptive NK cells, and a unique NK cell subset that is expanded and characterized by upregulation of CX3CR1, TBX21, MYOM2, DUSP1, and ZFP36L2, and negatively correlated with cognitive function in AD patients. Pseudo-temporal analysis revealed that this unique NK cell subset was at a late stage of NK cell development and enriched with transcription factors TBX21, NFATC2, and SMAD3. Together, our study identified a distinct NK cell subset and its potential involvement in AD.

Background Due to the increasingly aging population in China and the changes in social and family structure, older adults’ care problems are becoming more and more prominent. To meet the home care needs of urban older adults, the Chinese government has launched Internet-Based Home Care Services (IBHCS). Although this model innovation can significantly relieve care problems, more and more evidence shows that there are many barriers in the process of IBHCS supply. The current literature is mostly from the perspective of the service users, and there are very few studies on the experience of service providers. Methods In this study, we took a qualitative phenomenological approach and used semi-structured interviews to investigate service providers’ daily experiences and the barriers they encounter. A total of 34 staff from 14 Home Care Service Centers (HCSCs) were included. Interviews were transcribed and analyzed using thematic analysis. Results We identified the barriers that service providers encounter in IBHCS supply: (1) bureaucratic repression: unreasonable policy plans, harsh assessment, excessive paperwork, different preferences of government leaders, and obstacles caused by COVID-19 control lead to a shift of focus in their work; (2) profitability crisis in the market: high service costs, dampened effective demand, government intervention in setting prices, and parent companies’ excessively high sales targets hinder the service supply process; (3) client-related challenges: the crisis of confidence, the dilemma of popularizing new technology, and communication barriers lead to rejection by older adults; (4) job dissatisfaction: low and unstable salary, heavy tasks, poor social acceptance of occupations, and lack of professional value reduce work enthusiasm. Conclusion We have investigated the barriers faced by service providers when providing IBHCS for urban older adults in China, providing empirical evidence in the Chinese context for the relevant literature. In order to provide IBHCS better, it is necessary to improve the institutional environment and market environment, strengthen publicity and communication, target customer needs, and adjust the working conditions of front-line workers.

Background Neuromyelitis optica spectrum disorder (NMOSD) is an autoantibody-triggered central nervous system (CNS) demyelinating disease that primarily affects the spinal cord, optic nerves and brainstem. Among the first responders to CNS injury, microglia are prominent players that drive NMOSD lesion formation. However, the key molecular switches controlling the detrimental activity of microglia in NMOSD are poorly understood. CD22 governs the activity of innate and adaptive immunity. In this study, we investigated to what extent and by what mechanisms CD22 may modulate microglial activity, neuroinflammation and CNS lesion formation. Methods To determine the expression profile of CD22 in NMOSD, we performed single-cell sequencing and flow cytometry analysis of immune cells from human peripheral blood. We investigated the potential effects and mechanisms of CD22 blockade on microglial activity, leukocyte infiltration and CNS demyelination in a mouse model of NMOSD induced by injection of NMOSD patient serum-derived AQP4-IgG and human complement. Results Single-cell sequencing and flow cytometry analysis revealed that CD22 was expressed in B cells, neutrophils, monocytes and microglia-derived exosomes in human peripheral blood from NMOSD patients and controls ( n  = 5 per group). In a mouse model of NMOSD, CD22 was expressed in B cells, neutrophils, monocytes and microglia ( n  = 8 per group). In NMOSD mice, CD22 blockade significantly increased the number of CNS lesions, astrocyte loss and demyelination, accompanied by increased inflammatory activity and phagocytosis in microglia. Furthermore, the detrimental effects of CD22 blockade were significantly alleviated in NMOSD mice subjected to depletion of microglia or Gr-1 + myeloid cells, suggesting the involvement of microglia and peripheral Gr-1 + myeloid cells. Additionally, CD22 blockade also led to significantly reduced phosphorylation of SYK and GSK3β in NMOSD. Notably, the detrimental effects of CD22 blockade were greatly diminished in NMOSD mice receiving the phosphorylated SYK inhibitor R406. Conclusions Our findings revealed a previously unrecognized role of CD22 as a key molecular switch that governs the detrimental effects of microglia and Gr-1 + myeloid cells in NMOSD, which paves the way for the future design of immune therapies for NMOSD. Graphical abstract

BackgroundResults from our recent study demonstrate that sphingosine-1-phosphate receptor 1 (S1PR1) modulation improves microvascular hemodynamics after cerebrovascular thrombosis. This study was to determine the microvascular hemodynamic effects of a sub-thrombolytic dose of tPA combined with a selective S1PR1 modulator ozanimod in a mouse model of cerebrovascular thrombosis.MethodsMicrovascular circulation in mice was monitored in vivo by two-photon microscopy. Thrombosis was induced in cortical arterioles by laser irradiation. Arteriolar flow velocity was measured by line-scanning following plasma-labeling with fluorescein-dextran.ResultsLaser‐induced thrombosis led to a persistent reduction of flow velocity in cortical arterioles. Sub-thrombolytic dose of tPA along with vehicle control did not improve the flow velocity in cortical arterioles following thrombosis. In contrast, a sub-thrombolytic dose of tPA along with ozanimod dramatically restored flow velocity in cortical arterioles following thrombosis. Ozanimod did not affect coagulation and bleeding time. Notably, ozanimod reduced thrombus volume without altering microvascular lumen diameter. In addition, ozanimod reduced leukocyte components within the thrombus.ConclusionsThese findings demonstrate that the thrombolytic effect of a sub-thrombolytic dose of tPA is markedly enhanced by S1PR1 modulation, implying that S1PR1 modulation may improve the therapeutic benefit of low-dose tPA in patients with acute ischemic stroke.

This research covers a multi-dimensional investigation into accessibility barriers in care services for older people with disabilities in rural China. In-depth interviews with 13 rural disabled older people in China were conducted using qualitative methods. Based on a welfare pluralism approach, the results showed that in comparison with urban areas, care services for disabled older populations in rural areas are more subject to social barriers. This can be seen in the limited state (lack of resources, rigorous eligibility qualifications, uneven distribution, and irregular implementation); the absent market (low levels of consumption, high cost pressures, self-exclusion, and traditional cultural constraints); absent NGOs and volunteers (difficulties in access for NGOs and volunteers outside the area and formation difficulties of local NGOs and volunteers); as well as low-quality care in households and communities (unprofessional care from the spouse, unsustainable care from children, and unavailable community-based care). A multi-subject support network should be established to remove accessibility barriers to care services for older people with disabilities in rural areas through active intervention and interaction. The results of the research provide insights that will aid in the formulation of future social care service plans and health policies for rural older people with disabilities.

An independent set is a set of vertices in a graph in which no two vertices are adjacent to each other. The maximum weighted independent set is the independent set with the largest sum of weights in a weighted graph. Considering that existing methods are inefficient when computing the maximum weighted independent set, we propose a combined neighbor reduction rule and a loss value-based greedy strategy to improve the efficiency and increase the weight of the independent set. Additionally, we propose the efficient approximate algorithms for the maximum weighted independent set on dynamic graphs. We decompose the weight change problem into five cases and propose corresponding strategies for each case. Finally, we conduct experiments on 8 real-world datasets to verify the effectiveness and efficiency of the proposed methods.

Intracerebral hemorrhage (ICH) is a devastating form of stroke with a lack of effective treatments. Following disease onset, ICH activates microglia and recruits peripheral leukocytes into the perihematomal region to amplify neural injury. Bruton's tyrosine kinase (BTK) controls the proliferation and survival of various myeloid cells and lymphocytes. However, the role of BTK in neuroinflammation and ICH injury remains poorly understood. Peripheral blood samples were collected from ICH patients and healthy controls to measure BTK expression profile in immune cell subsets. C57BL/6 mice were used to measure BTK expression and the activity of immune cell subsets following ICH induction. Neurological tests, brain water content, Evans blue leakage, MRI were used to assess the therapeutic effects of ibrutinib on ICH injury. Flow cytometry was used to investigate immune cell infiltration and microglial activity. Microglia were depleted using a CSF1R inhibitor PLX5622. Gr-1 myeloid cells and B cells were depleted using monoclonal antibodies. Microglia-like BV2 cells were cultured to test the effects of BTK inhibition on these cells. In humans and mice, we found that BTK was remarkably upregulated in myeloid cells after ICH. Inhibition of BTK using ibrutinib led to reduced neurological deficits, perihematomal edema, brain water content and blood-brain barrier disruption. BTK inhibition suppressed the inflammatory activity of microglia and brain infiltration of leukocytes. In contrast, BTK inhibition did not alter the counts of peripheral immune cells other than B cells. Further, the depletion of microglia or Gr-1 myeloid cells ablated the protective effects of BTK inhibition against ICH injury. Notably, the depletion of B cells did not alter the protective effects of BTK inhibition against ICH injury. This suggests that the benefit of BTK inhibition in ICH mainly involves its impact on microglia and Gr-1 myeloid cells. Our findings demonstrate that BTK inhibition attenuates neuroinflammation and ICH injury, which warrants further investigation as a potential therapy for ICH.

Neuromyelitis optica spectrum disorder (NMOSD) is an antibody-mediated neurological inflammatory disease. As a G protein-coupled receptor, formyl peptide receptor 2 (FPR2) orchestrates innate and adaptive immunity. Yet the precise role of FPR2 in neuroinflammation is poorly understood. Peripheral blood samples were collected from patients with NMOSD and healthy controls. Single-cell RNA sequencing (scRNA-seq) and flow cytometry were employed to assess the expression of FPR2 in immune cell subsets. We used a mouse model of NMOSD to examine the therapeutic potential and underlying immune mechanisms of an FPR2 antagonist Quin-C7. MRI and immunostaining were performed to quantify central nervous system injury. ScRNA-seq and flow cytometry analyses revealed that FPR2 was expressed in various myeloid and lymphoid cell types in patients with NMOSD and a mouse model of NMOSD. In NMOSD mice, mouse formyl peptide receptor 2 (mFpr2) was mainly upregulated in microglia. Administration of Quin-C7 led to reduced brain lesion volume, astrocyte loss and demyelination in NMOSD mice. Further, FPR2 antagonism reduced the inflammatory activity of microglia and lymphocyte infiltration into the brain. Notably, depletion of microglia using a CSF1R inhibitor diminished the protective effects of FPR2 antagonism, suggesting that microglia contribute to the benefit of FPR2 antagonism in NMOSD. In contrast, genetic deficiency of T and B cells or antibody depletion of NK cells did not affect the benefit of FPR2 antagonism. Collectively, our findings revealed a previously unrecognized role of FPR2/mFpr2 in control of microglia activity during neuroinflammation, implying that FPR2 antagonism may serve as a viable therapeutic approach to restrict detrimental neuroinflammation and warrant further investigation.

Cell death is an essential biological process for physiological growth and development. Three classical forms of cell death—apoptosis, autophagy, and necrosis—display distinct morphological features by activating specific signaling pathways. With recent research advances, we have started to appreciate that these cell death processes can cross-talk through interconnecting, even overlapping, signaling pathways, and the final cell fate is the result of the interplay of different cell death programs. This review provides an insight into the independence of and associations among these three types of cell death and explores the significance of cell death under the specific conditions of human diseases, particularly neurodegenerative diseases and cancer.